1. Field of the Invention
This invention relates to a method and apparatus for electrically stimulating the certain nerves for the prevention or interruption of bouts of myocardial ischemia, either automatically or upon external command by the patient or physician.
2. Description of the Prior Art
Vagal stimulation for the treatment of supraventricular arrhythmias, angina pectoris, and heart failure with an automatic, permanently implantable, medical device has been reported in the literature at least as far back as the early 1960's. The paper "Vagal Tuning" by Bilgutay et al in the Journal of Thoracic and Cardiovascular Surgery, Vol. 56, No. 1, July, 1968, pp. 71-82, described the concepts of vagal stimulation in the treatment of supraventricular arrhythmias, angina pectoris, and heart failure employing an implantable vagal stimulator. Vagal stimulation was effected through the application of electrical stimulation to the vagus nerve by silastic coated, bipolar electrodes (of the type disclosed in Medtronic U.S. Pat. No. 3,421,511) surgically placed around the intact nerve or nerves. Bilgutay et al. designed and employed three different models of vagal stimulators, the first one having a magnetic switch by which it could be turned on or off from outside the body to study the effects of long term stimulation, the second type also implantable but powered from outside by induction using rf frequency, and the third, external type triggered by the R-wave of the subject's electrocardiogram to provide stimulation only upon an achievement of a certain heart rate. Bilgutay et al. found that when a pulsatile current with a frequency of ten pulses per second and 0.2 milliseconds pulse duration was applied to the vagus nerve, long term effective stimulation could be achieved, and also found that by increasing only the voltage amplitude and current, more predictable changes on the electrocardiogram could be obtained. The heart rate could be decreased down to half the resting rate while still preserving sinus rhythm with up to 9 volts applied voltage. Atrio-Ventricular (AV) conduction dissociation and third degree heart block resulted at amplitudes exceeding 9 volts, and complete asystole with vagal escape resulted when the applied voltage exceeded 20 volts. Low amplitude vagal stimulation was successfully employed to control induced tachycardias and ectopic beats, and the authors noted other advantages of vagal stimulation in alleviating adverse effects of available drug therapies.
Other investigators reported treatment of angina pectoris and paroxysmal atrio-ventricular junctional or supraventricular tachycardias through application of carotid sinus nerve stimulation employing the Medtronic Angistat carotid sinus nerve stimulator (csns) then available from Medtronic, Inc. in papers such as "Carotid Sinus Nerve Stimulation in the Treatment of Angina Pectoris and Supraventricular Tachycardia", California Medicine, 112:41-50, March, 1970, in papers reference therein. These papers describe the system for effecting carotid sinus nerve stimulation by a radio frequency responsive stimulator activated by the patient at will in response to the patient's awareness of the onset of angina and/or supraventricular tachycardia.
Angina pectoris is a chest pain that accompanies and is indicative of myocardial ischemia. Oftentimes myocardial ischemia is "silent" and not accompanied by angina pectoris, in either case, ischemia is an oxygen starvation of the myocardium that is a precursor to myocardial infarction or the death of the starved myocardial cells. To protect these cells, the cells' oxygen demand must be reduced (or coronary flow increased).
The oxygen demands of the heart are not simply a function of the external work of the heart, that is, the product of arterial pressure and cardiac output. The development by the ventricles of pressure (more strictly speaking, tension) has a high oxygen cost. In addition to tension, the level of myocardial contractility, that is the inotropic or contractual state of the myocardium, is a second important determinant of the heart's oxygen needs. A third factor, of course, is that the heart's oxygen consumption is a function of cardiac frequency--the number of times the heart contracts per unit of time. A number of other physiologic variables have been studied, but none even approach in importance the three factors mentioned above--tension, contractility and heart rate--in the determination of myocardial oxygen consumption.
It is generally appreciated that angina pectoris results from an imbalance between the heart's oxygen needs and the oxygen supply. In the large majority of patients this imbalance results from a defect in the delivery of oxygen to the myocardium as a consequence of obstruction in the coronary vascular bed secondary to atherosclerosis or coronary spasm. In other patients, however, this imbalance results to a significant extent from increased myocardial oxygen demands, as occurs in aortic stenosis, thyrotoxicosis and tachycardia. Ideal therapy for severe myocardial ischemia would be to restore the balance between supply and demand in as a physiologic a manner as possible--by increasing oxygen delivery when it is limited, and by reducing oxygen demands when these are excessive. In practice, it may be difficult or impossible to increase oxygen delivery, particularly in patients with diffuse severe atherosclerosis. Some researchers have sought to relieve angina pectoris by reducing myocardial oxygen consumption through stimulation of the vagus nerve.
Investigators focused upon the use of carotid sinus nerve stimulation in the treatment and control of angina pectoris for regulation of the patient's blood pressure, and observed that the effect of the application of carotid sinus nerve stimulation provided a safe means for initiating reflex vagal activity which in turn effected a slowing in a patient's heart rate or even terminating a supraventricular tachycardia.
In U.S. Pat. No. 3,650,277, it was also proposed to stimulate the left and right carotid sinus nerves in response to the detection of elevated mean arterial blood pressure to alleviate hypertension.
Thus it is well known that the application of stimulation to the right or left carotid sinus nerves, either directly or indirectly, has the effect of lowering blood pressure which in turn decreases ischemia and attendant angina pectoris symptoms, with the danger that an important brady-arrhythmia may be induced in the process.
Difficulties in detecting ischemia and providing proper amplitudes, frequencies and duration of the electrical stimulation has effectively led to the near abandonment of this therapy in recent years. It has also been shown that many important and significant episodes of ischemia may not be detected by the patient and further cardiac damage may follow. This limits the use of patient activator systems.